DNA aneuploidy and dysplasia in oral potentially malignant disorders: Association with cigarette smoking and site

Pentenero, Monica; Giaretti, Walter; Navone, Roberto; Demurtas, Anna; Rostan, Isabella; Bertolusso, Giorgio; Broccoletti, Roberto; Arduino, Paolo Giacomo; Malacarne, Davide; Gandolfo, S

doi:10.1016/j.oraloncology.2009.03.008

Cited by 36 publications

(37 citation statements)

References 28 publications

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“…These data appear in agreement with the concept of field effect in oral carcinogenesis (Braakhuis et al, 2003;Bremmer et al, 2008;Tabor et al, 2001;Van der Waal, 1997). The data obtained for the nondysplastic OPMLs, in particular, were in agreement with previous literature reports including two studies from our group using an independent patient population (Donadini et al, 2010;Pentenero et al, 2009;Saito, 1995). These data were, however, in contrast with other studies, which did not detect DNA aneuploid sublines in such lesions (Kahn et al, 1992;Saito, 1998).…”

Section: Discussionsupporting

confidence: 92%

“…The incidence of DNA aneuploidy by FCM reported in the literature ranges from about 10% to 40% for dysplastic OPMLs (Donadini et al 2010;Pentenero et al 2009;Saito et al, 1998Saito et al, , 1991Saito et al, , 1995Seoane et al, 1998) and up to about 80% for OSCCs (Donadini et al, 2010;Pentenero et al 2009;Hemmer, 1990Hemmer, , 1997. These values may strongly depend on the tissue material type (paraffin embedded or fresh-frozen) and DNA FCM resolution.…”

Section: Discussionmentioning

confidence: 99%

“…The role of chromosomal instability during the genesis and progression of oral cancer has clearly been indicated by several studies but still our understanding of the molecular mechanisms is relatively poor. Analyses were performed with the use of different techniques including loss of heterozygosity (Braakhuis et al, 2004;Bremmer et al, 2008;Graveland et al, 2011;Lydiatt et al, 1998;Mithani et al, 2007;Partridge et al, 1997;Tsantoulis et al, 2007), comparative genomic hybridization and gene expression array (Bremmer et al, 2008;Cha et al, 2011;Garnis et al, 2009;Liu et al, 2006Liu et al, , 2011Smeets et al, 2009;Snijders et al, 2005;Squire et al, 2002;), in situ hybridization (Nees et al, 1993;Voravud et al, 1993), immunohistochemistry (Nees et al, 1993), multiplex ligation-dependent probe amplification (Bremmer et al, 2008;Cha et al, 2011;Liu et al, 2006), DNA image cytometry (Bremmer et al, 2008;Diwakar et al, 2005) and DNA flow cytometry (DNA FCM) (Donadini et al, 2010;Hemmer, 1990Hemmer, , 1997Pentenero et al, 2009;Saito, 1998Saito, , 1991Saito, , 1995Seoane et al, 1998). DNA FCM was often adopted as a useful technique for detecting the presence of DNA aneuploid sublines in several human predisposing and preneoplastic lesions such as Barrett's esophagus (Reid et al, 2000), ulcerative colitis (Rabinovitch et al, 1999;Risques et al, 2008), colorectal adenomas (Giaretti et al, 1994) and oral lesions …”

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confidence: 99%

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Model of Chromosomal Instability in Oral Carcinogenesis and Progression

Giaretti¹

2012

Oral Cancer

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Model of Chromosomal Instability in Oral Carcinogenesis and Progression

Giaretti¹

2012

Oral Cancer

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“…Therefore, our systems biology approach would be superior to understand the complex nature of exposure and its impacts. Finally, to generate a more complete risk assessment, genotoxicity test, such as aneuploidy and chromosomal instability assays could be incorporated in future studies (Giaretti et al, 2012a,b; Pentenero et al, 2009). …”

Section: Discussionmentioning

confidence: 99%

In vitrosystems toxicology approach to investigate the effects of repeated cigarette smoke exposure on human buccal and gingival organotypic epithelial tissue cultures

Schlage

Iskandar

Kostadinova

et al. 2014

Toxicology Mechanisms and Methods

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Smoking has been associated with diseases of the lung, pulmonary airways and oral cavity. Cytologic, genomic and transcriptomic changes in oral mucosa correlate with oral pre-neoplasia, cancer and inflammation (e.g. periodontitis). Alteration of smoking-related gene expression changes in oral epithelial cells is similar to that in bronchial and nasal epithelial cells. Using a systems toxicology approach, we have previously assessed the impact of cigarette smoke (CS) seen as perturbations of biological processes in human nasal and bronchial organotypic epithelial culture models. Here, we report our further assessment using in vitro human oral organotypic epithelium models. We exposed the buccal and gingival organotypic epithelial tissue cultures to CS at the air–liquid interface. CS exposure was associated with increased secretion of inflammatory mediators, induction of cytochrome P450s activity and overall weak toxicity in both tissues. Using microarray technology, gene-set analysis and a novel computational modeling approach leveraging causal biological network models, we identified CS impact on xenobiotic metabolism-related pathways accompanied by a more subtle alteration in inflammatory processes. Gene-set analysis further indicated that the CS-induced pathways in the in vitro buccal tissue models resembled those in the in vivo buccal biopsies of smokers from a published dataset. These findings support the translatability of systems responses from in vitro to in vivo and demonstrate the applicability of oral organotypical tissue models for an impact assessment of CS on various tissues exposed during smoking, as well as for impact assessment of reduced-risk products.

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“…Several recent studies have reported the potential use of DNA ploidy analysis to predict the behaviour of oral PMD [6][7][8][9][10][11][12]. Aneuploidy in oral dysplastic lesions, as detected by DNA image cytometry, was found to be indicative of a high risk of OSCC development [10].…”

Section: Introductionmentioning

confidence: 99%

Correlation Between Dysplasia and Ploidy Status in Oral Leukoplakia

Zyl

Heerden

Langenegger

et al. 2012

Head and Neck Pathol

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Oral leukoplakia and other potentially malignant disorders (PMD) may progress to oral squamous cell carcinoma (OSCC). The gold standard for assessing the potential for malignant transformation remains histologic examination with the aim of grading the dysplastic changes. However, not all lesions with dysplasia will progress to OSCC. DNA ploidy has been suggested as a method to predict the clinical behaviour of PMD. This study reports on the use of high-resolution flow cytometry to determine the ploidy status of formalin-fixed, paraffin-embedded material from PMD compared to their dysplasia grade on histology. Aneuploidy was found in 13 % of mild, 31 % of moderate, and 54 % of severe dysplasia cases. This difference was statistically significant (p = 0.011). The differences in ploidy status were more significant when grouping the dysplasia into low-risk and high-risk categories (p = 0.008). These findings indicate that the ploidy status of PMD as determined by high-resolution flow cytometry may be of value in predicting biological behaviour in PMD such as leukoplakia.

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DNA aneuploidy and dysplasia in oral potentially malignant disorders: Association with cigarette smoking and site

Cited by 36 publications

References 28 publications

Model of Chromosomal Instability in Oral Carcinogenesis and Progression

Model of Chromosomal Instability in Oral Carcinogenesis and Progression

In vitrosystems toxicology approach to investigate the effects of repeated cigarette smoke exposure on human buccal and gingival organotypic epithelial tissue cultures

Correlation Between Dysplasia and Ploidy Status in Oral Leukoplakia

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